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The potential role of DEK over-expression in the radiation response of head and neck cancer

The potential role of DEK over-expression in the radiation response of head and neck cancer

作     者:Hui Xiao Bismarck Odei Steven K.Clinton Darrion L.Mitchell Hui Xiao;Bismarck Odei;Steven K. Clinton;Darrion L. Mitchell

作者机构:Department of Radiation OncologyThe Ohio State UniversityOH43210USA The Ohio State University Comprehensive Cancer CenterThe Ohio State UniversityOH43210USA Division of Medical OncologyDepartment of Internal MedicineThe Ohio State UniversityOH43221USA 

出 版 物:《Radiation Medicine and Protection》 (放射医学与防护(英文))

年 卷 期:2021年第2卷第1期

页      面:28-32页

学科分类:1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基  金:This work was supported by the National Cancer Institute at the National Institutes of Health K12 Grant(#K12CA133250) 

主  题:HPV Oropharynx Radiation DEK 

摘      要:Objective:To determine if DEK over-expression is associated with radiation resistance in HPV positive head and neck cancer ***:Control and DEK over-expressing keratinocytes and an HPV positive head and neck cancer cell line respectively were irradiated with 2–10 Gy and the impact on cell survival,γ-H2AX(a marker of DNA damage)and RAD51(homologous recombination)were analyzed via clonogenic assays,and immunofluorescence measurements ***:Upon exposure to increasing doses of radiation,DEK over-expression in keratinocytes at 2,4(P0.05,P0.05),and 10 Gy(P0.01)and an HPV positive head and neck cancer cell line at 2,4,8,and 10 Gy(P0.01)led to improved clonogenic cell *** parallel,irradiation decreased the percent ofγ-H2AX foci at 6,24,and 48 h post-irradiation(P0.05,P0.05,and P0.01 respectively)in NIKS,and at 0,6,24,48 h post-irradiation(P0.05,P0.05,P0.01,P0.01)in C-SCC1 cells but enhanced the percent of RAD51 foci in both DEK over-expressing cell lines relative to their respective control cells at all times points(P0.01).Conclusion:These results suggest DEK over-expression contributes to radio-resistance in HPV positive head and neck cancer cells,potentially by improving repair of DNA double strand breaks through homologous *** molecular mechanisms and relevance to in vivo responses needs further investigation.

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